There is a marked increase in the prevalence of obesity worldwide, In this regard, onesity is associated with a considerable morbidity and mortality. A large component of this morbidity and mortality is through an increased risk for cardiovascular events, which is in-part attributed to the association between obesity and hypertension or cardiac dysfunction. In the present thesis I conducted a series of studies designed to advance our understanding of the role of an obesity-associated sedentary lifestyle or insulin resistance in promoting the development of hypertension or left ventricular (LV) diastolic dysfunction. Despite the particular importance of salt-sensitivity in contributing toward increases in BP in groups of African descent, the role of obesity or insulin resistance in mediating this effect in this ethnic group is uncertain. In addition, whether this effect translates into changes in central aortic BP is unknown. I therefore aimed to determine whether obesity or insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]) is independently associated with salt intake (24-hour urinary Na+/K+) blood pressure (BP) relationships in 331 participants from a community sample of African ancestry not receiving treatment for hypertension and whether this association occurs in both brachial and central aortic BP. Although log HOMA-IR was not independently associated with BP, with adjustments including diabetes mellitus and the individual terms, an interaction between log HOMA-IR and urinary Na+/K+ was associated with 24-hour, day systolic (p<0.05) and 24- hour, day and night diastolic (p<0.002 to p<0.001) BP. Neither aortic augmentation pressure, aortic augmentation index, central aortic pulse pressure not aortic pulse wave velocity were independently associated with an interaction between log HOMA-IR and urinary Na+/K+ The multivariate adjusted relationship between urinary Na+/K+ and night diastolic BP increased across tertiles of HOMA-IR (Tertile 1: -coefficient=-0.79±0.47; Tertile 2: - coefficient=0.65±0.35; Tertile 3: -coefficient=1.03±0.46, p<0.05 tertiles 3 and 2 vs 1). In conclusion, insulin resistance is independently associated with the relationship between salt intake, as indexed by urinary Na+/K+, and ambulatory BP in groups of African descent. Thus, iv in persons of African ancestry, salt-sensitivity may depend in-part on the presence of insulin resistance. These effects of insulin resistance cannot be accounted for by actions on central aortic haemodynamics. In overweight or obese individuals, whether the beneficial effects of exercise training on BP can be explained by decreases in aortic systolic pressure augmentation is uncertain. Therefore I aimed to determine the impact of 6 weeks of exercise training ( 3 days/week, on a stationary bike and/or treadmill) either preceded (n=19) or followed by (n=16) a 6 week control period of no exercise, on aortic augmentation pressure and index and central aortic and brachial BP in 35 sedentary or recreationally active young-to-middle-aged overweight (40%) or obese (60%) individuals. Aortic augmentation pressure (AP), aortic and peripheral augmentation indices (AIx), central aortic BP (SphygmoCor) and brachial BP were determined before and after exercise training and a control period. Peak oxygen consumption (cardiorespiratory fitness) increased (p=0.0001) from 27.0±5.1 to 28.8±5.8ml.kg-1.min-1 after 6 weeks of exercise. Exercise training decreased brachial systolic BP and diastolic BP from 142±8/94±8 mm Hg to 134±11/86±11 mm Hg (p<0.005/p<0.005); whereas no changes were observed after the control period. Neither AP (baseline: 9.2±4.2 mm Hg; after 6 weeks training: 8.7±6.1 mm Hg), aortic AIx (Baseline: 24.6±11.0%; after 6 weeks training: 22.7±11.1%), nor peripheral AIx (Baseline: 81.4±16.7%; after 6 weeks training: 76.4±16.5%) were modified by exercise training. Although aortic systolic BP decreased after exercise training (132±8 mm Hg to 124±12 mm Hg, p<0.002), these changes were accounted for by decreases in MAP. In conclusion, overweight or obese individuals, although short-term aerobic exercise training which improved cardiorespiratory fitness, may decrease aortic and brachial BP, these effects are not attributed to alterations in aortic systolic pressure augmentation. Considering the effects of obesity on the vasculature the repercussions on the function of the heart itself should also be considered. In this regard whether the relationship between obesity and abnormalities in LV diastolic function can be accounted for by insulin resistance independent of adiposity indexes, or LV mass or remodelling is uncertain. In 361 participants (24% overweight, 38% v obese) from a South African community sample of black African descent not receiving treatment for hypertension, I evaluated LV dimensions and diastolic function (E/A) with echocardiography, HOMA-IR, and nurse-derived conventional BP. Log HOMA-IR was associated with E/A independent of waist circumference and additional confounders (p<0.005). The independent impact of log HOMA-IR on E/A ( -coefficient=-0.11±0.04, p<0.005) was similar to the effects of conventional DBP ( -coefficient=-0.12±0.04, p<0.01), but less than that of age ( -coefficient=-0.52±0.05, p<0.0001). Although, log HOMA-IR was independently related to relative wall thickness (partial r=0.16, p<0.005), the multivariate adjusted relationship between log HOMA-IR and E/A was not altered by further adjustments for either relative wall thickness ( -coefficient=-0.10±0.04, p<0.01) or LV mass index ( - coefficient=-0.11±0.04. p<0.01). In conclusion, insulin resistance is associated with a decreased LV diastolic function independent of adiposity indices and LV mass or remodelling. Hence insulin resistance may be an important pathophysiological mechanism responsible for the abnormalities in LV diastolic function. Although exercise training has consistently been shown to be unable to improve obesity-associated decreases in LV diastolic function as assessed using change function measurements, the effects of exercise training on LV diastolic myocardial function as assessed using Tissue Doppler Imaging (TDI) are uncertain. Hence, in 32 overweight (n=11) or obese (n=21), sedentary or recreationally active men and women (30–57 years), I aimed to determine the impact of 6 weeks of exercise training either preceded (n=16) or followed by (n=16) a 6 week control period on TDI-derived parameters of LV diastolic function (e’, e’/a’, E/e’). Cardiorespiratory fitness (peak oxygen consumption, VO2peak), LV diastolic function (E/A, TDI e’, e’/a’ and E/e’) (echocardiography) and body weight were determined at baseline and after the control and exercise training periods. Baseline measures of diastolic function were comparable with those noted in overweight and obese participants from a community sample (n=245) and 56% (n=18) had baseline e’ values (early diastolic abnormalities) that were below the lower 95% confidence intervals of a lean and healthy cohort (n=60) of the community sample. Exercise training increased peak oxygen consumption from 27.4±4.9 to 29.4±5.8 ml.kg-1.min-1 (p=0.0001); but had no effect on body mass index (p=0.99). No changes in TDI indices of LV diastolic function were observed after exercise training in all participants (e’: p=0.74, a’: p=0.98, e’/a’: p=0.85; E/e’: p=0.26), in participants with abnormal e’ values (n=18)(e’: p=0.99, a’: p=0.96, e’/a’: p=0.91; E/e’: p=0.97) or in obese participants only (n=21)(e’: p=0.67, a’: p=1.00, e’/a’: p=0.78; E/e’: p=0.11. Thus, exercise training alone, despite producing an improved cardiorespiratory fitness is unable to improve obesityassociated decreases in LV diastolic myocardial function In conclusion, the results of my thesis suggest the following: In groups of African ancestry, obesity effects on salt sensitive hypertension or abnormalities of LV diastolic function may in-part be accounted for by insulin resistance. In addition, short-term, regular exercise in overweight and obese individuals without weight loss, but with an increased cardiorespiratory fitness, is unable to influence those large vessel characteristics that contribute to BP or LV diastolic function. Thus, studies that assess the impact of approaches that increase insulin sensitivity on BP-responses to salt intake and LV diastolic function in obese individuals are warranted, but short-term exercise training alone may not achieve this goal.

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